Paracrine and autocrine functions of the placenta: a key to the success of viviparity?

 

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Summary

The evolution of specific nuclear transcriptional regulators has endowed tissues of the reproductive system with responsiveness to small hydrophobic compounds such as steroids. Steroids are widely distributed in Nature and their distribution in prokaryotes and eu-karyotes has given rise to the concept that their hormonal role came about by target organ specialization and not by the evolution of steroids themselves. Specific nuclear receptors for progesterone in the uterus are prominent during the establishment and maintenance of pregnancy. Anti-progesterone antagonists which interfere with receptor-mediated DNA activation abrogate pregnancy and thus emphasize the functional importance of the pathways by which the effects of progesterone as an extracellular signal are transduced. Comparative studies show that progesterone itself can be ovarian or placental in origin. This seems to reflect the evolution of different mechanisms of endocrine function rather than any obvious selective advantage being associated with the source of hormone secretion. For this reason, the question of whether the endocrine function of the placenta is obligatory for the adoption of viviparity in mammals is far from certain, and should be considered as an evolutionary option rather than a sine qua non. Of growing importance is the idea that the interaction between trophoblast and endometrial cells controls the degree of invasiveness at implantation and immunoreac-tivity. Both of these processes require exquisitely sensitive forms of regulation and current studies suggest that it is the acquisition of paracrine and autocrine functions by the placenta that is a critical step in the adoption of viviparity as the preferred mode of reproduction in mammals.